How to Image the Dilated Right Ventricle

From the Philadelphia Adult Congenital Heart Disease Program, A Joint Program of the Hospital of the University of Pennsylvania and Children’s Hospital of Philadelphia (S.L.P.); and CMR Unit, Royal Brompton Hospital and Imperial College, London, United Kingdom (P.J.K.).

From the Philadelphia Adult Congenital Heart Disease Program, A Joint Program of the Hospital of the University of Pennsylvania and Children’s Hospital of Philadelphia (S.L.P.); and CMR Unit, Royal Brompton Hospital and Imperial College, London, United Kingdom (P.J.K.).

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Clinical Vignette

A 32-year-old man presented to his local emergency department with a sudden onset of palpitations and was found to be in atrial flutter at a ventricular rate of 145 bpm. He spontaneously converted to sinus rhythm in the emergency department. In sinus rhythm, he was asymptomatic, and his physical examination demonstrated no jugular venous distention, a fixed split second heart sound, and a I/VI early peaking systolic ejection murmur loudest over the left upper sternal border. His ECG demonstrated sinus rhythm with an incomplete right bundle branch block.

A transthoracic echocardiogram (TTE) was performed to assess for structural heart disease given his episode of atrial flutter, physical examination, and ECG findings. His TTE demonstrated a moderately dilated right ventricle (RV) based on qualitative assessment (Figure 1). Once a dilated RV was identified, the rest of the echocardiographic examination paid particular attention to identifying causes for his RV dilation (Table 1). There was evidence of RV volume overload with no evidence of RV pressure overload (Figure 2). No obvious cause for RV volume loading was identified with structurally normal right-sided valves, only mild tricuspid regurgitation and trace pulmonary regurgitation. The intra-atrial septum was not well seen, but there was no obvious atrial-level shunt. The tricuspid regurgitant jet was consistent with a right ventricular systolic pressure within normal limits ruling out RV pressure overload. There were no regions of focal RV akinesis or dyskinesis to suggest arrhythmogenic RV cardiomyopathy.